摘要
目的:探讨姜黄素(curcumin)预防高原缺氧大鼠认知功能障碍的电生理机制。方法:将30只成年雄性SD大鼠随机分为健康对照组、模型组(Model组)、姜黄素[按体重60mg/(kg.d)]治疗组(curcumin组)。造模后,检测脑片水平的海马的LTP变化,并运用膜片钳技术检测海马CA1区神经元的电生理变化。结果:(1)给予HFS刺激后各组均可诱发LTP并持续1h以上,与对照组比较模型组组HFS刺激后LTP明显被抑制(P<0.05),姜黄素可减轻缺氧所致的LTP抑制(P<0.05);(2)高原缺氧使海马CA1神经元阈电位升高,动作电位(AP)数量减少,兴奋性降低,姜黄素干预可明显减轻高原缺氧对细胞神经元的抑制。结论:姜黄素可显著改善高原缺氧大鼠认知功能障碍,其可能机制是通过维持海马CA1细胞的兴奋性减轻高原缺氧对认知功能的损伤。
Objective: To investigate the electrophysiology mechanism of curcumin prevent hypobaric hypoxia -induced cognitive deficits. Methods: 30 male Sprague-Dawley rats(200± 20 g) were randomly divided into three groups with 10 rats in each group: Control group, Model group and Curcumin group. Hippocampal LTP was detected by electrophysiology method. Excitability of Hippocampal CA1 neuron was measured by whole-cell patch-clamp recordings in rat brain slices. Results: LTP inhibition in hippocampus caused by hypobaric hypoxia are markedly improved by administration of curcumin. The excitability of hippocampal CA 1 neurons is inhibitted by hypobaric hypoxia, and curcumin can maintain the excitability of neuron. Conclusions: Curcumin can prevent hypobaric hypoxia-induced cognitive deficits through maintain the excitability ofhippocampal CA1 neurons.
出处
《现代生物医学进展》
CAS
2011年第22期4229-4231,4239,共4页
Progress in Modern Biomedicine
关键词
高原缺氧
姜黄素
认知功能障碍
电生理
Hypobaric hypoxia
Curcumin
Cognitive deficits
Electrophysiology